We have previously observed that after addition of exogenous renin, angiotensin I generation is faster in plasma of hypertensive patients and patients with renal disease than in plasma of normotensive subjects. We have demonstrated that this increased reactivity of renin may be related to the deficiency of a circulating neutral lipid renin inhibitor. The purpose of this project is to identify circulating renin inhibitors and to determine if increased reactivity of exogenous renin in hypertensive and uremic plasma can be attributed to a deficiency of these inhibitors. To demonstrate an in vivo effect of renin inhibition, we will determine if lipids that inhibit renin in vitro also lower blood pressure in experimental renin dependent hypertension.